Normal visual input is indispensible to the development and maintenance of visual centers. Abnormal input to one eye achieved by lid-suture induces changes in this deprived eye as well as in centers connected with it. Recently, we have demonstrated a decreased density of synapses in the deprived visual cortex, which is consistent with the decreased activation of neurons observed in this cortex. The cortical changes can be meaningfully interpreted only if the impact of monocular deprivation on the fine structure of the dorsal nucleus of the lateral geniculate (subcortical relay center of the visual pathway) is understood. Since most of the deprivation studies were so far conducted in species with a strong binocular input, it is of no surprise that the observed postdeprivation changes in these animals were attributed to binocular competition. This competition is believed to be brought about by asymmetrical activation of the binocular center, which brings the deprived pathway into a competitive disadvantage with the undeprived one. Since the lid-sutured eye is entirely deprived of form vision, a deficient type of information is transmitted to the center, which can be expected to result in the disuse of elements involved. Which of the mechanisms is primarily responsible for postdeprivation changes cannot be resolved in species with a strong binocular input. An animal with a weak binocular input like the hooded rat is a more suitable object for investigation since in this species the binocular competition is unlikely to be the sole mechanism of postdeprivation changes. For that matter, the fine structure of the deprived dorsal nucleus of the lateral geniculate is proposed to be studied together with the metabolic activity in the visual pathway at the cortical and subcortical level.